Abstract
KC1 was administered orally to hyponatremic patients with and without edema. In these patients small to rather striking increases in the serum Na concn. were observed without the addition of exogenous sodium. The nature of the phenomenon is not wholly clarified but seems best explained by postulating a release of Na from cells in exchange for K. The estimated release of Na ion was of the order of 60-300m.eq. The actual change was probably in excess of these values since the extracellular volume was estimated to be only 20% of the body wt. in patients often massively edematous. In the edematous hyponatremic subject no significant change in renal excretion of Na or water was observed, after KC1 admn., even when serum Na levels were simultaneously raised towards normal. This occurred with both low and higher Na intakes. The hyponatremic patients studied seemed unable to metabolize K with normal facility and its admn. is therefore not without hazard; when compared to normal subjects the hyperkalemia produced seemed to be more profound and more prolonged. Moreover, with the doses employed in this study KC1 did not exert a diuretic action.